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Gerontologija 2008; 9(2):103–108
GERONTOLOGIJA
Theory and practice
Skin aging
Z. Mackiewicz, A. Rimkevičius
Institute of Experimental and Clinical Medicine at Vilnius University
Abstract
Irreversible skin aging changes usually begin early in the
second decade of life, though the external signs may be not
visible for a long time. Skin aging is a complex biological process resulting from both intrinsic, or genetically programmed,
changes that develop with time and extrinsic impacts caused by
environmental factors. A number of extrinsic factors often act
together with the physiological aging process. Extrinsic factors
that prematurely age the skin are repetitive facial expressions,
gravity, bad sleeping positions, smoking, etc. The external signs of skin aging are fine wrinkles, thin and transparent skin,
pigment spots, loss of underlying fat, sagging skin, dry skin
with or without itch, inability to sweat sufficiently, graying
hair, hair loss, unwanted hair, thinning of the nail plate, disappearance of the nail half-moons, ridges. Changes and reduction
of the blood vessels are an essential and permanent feature in
the skin of elderly individuals.
It is not possible to stop or even appreciably slow down the
intrinsic aging process, however everybody is able to attenuate
the signs of premature aging by protecting skin from the sun,
quitting smoking, eliminating harmful facial exercises, abolishing diseases influencing skin aging, etc.
Address: Z. Mackiewicz
Žygimantų str. 9, LT-01102 Vilnius, Lithuania
E-mail: [email protected]
Keywords:
skin, aging
Introduction
While age-related skin changes usually begin at twenties, the external signs of intrinsic aging may be not visible for decades. These signs are fine wrinkles, thin and
transparent skin, loss of underlying fat leading to hollowed cheeks and eye sockets, as well as a noticeable
loss of skin firmness on the hands and neck, shrink of
the skin due to bone loss, dry skin that may itch, inability
to sweat sufficiently to cool the skin, graying hair, hair
loss, unwanted hair, thinning of the nail plate, disappearance of nail half-moons, and ridges. Genes control how
quickly the normal aging process unfolds.
A number of extrinsic factors often act together with
the normal aging process to prematurely age the skin.
Often premature aging is caused by sun exposure. Other
external factors are repetitive harmful facial expressions,
gravity, bad sleeping positions, smoking, wrong diet,
etc.
Skin as an organ
Skin is the largest body organ of the integumentary
system that guards underlying muscles and organs. It
serves as a protective shield against harmful temperature,
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light, injury, and infection. Skin also stores water, fat, vitamin D, senses painful and pleasant stimulation. Human
skin is about 2 mm thick. On average, an adult has about
2 square meters of skin which weighs about 2.7 kg. The
outer skin layer, the epidermis, is a tough layer that contains melanin protecting against the rays of the sun and
giving the skin its colour, and elements of the immune
system. The second layer (located under the epidermis)
is called the dermis. It contains the network of blood vessels, nerve endings, sweat glands, sebaceous glands, hair
follicles, and hair muscles. Under these two skin layers
lies a fatty layer of subcutaneous tissue. Throughout the
body, the skin’s characteristics vary in thickness, colour,
texture, hair follicles. Asian and African race skin exhibits increased dermal thickness, collagen, and melanin
content as compared with Caucasian skin.
Physiological aging of the skin
Skin aging is a complex biological process resulting
from both intrinsic, or genetically programmed, aging that
occurs with time and extrinsic aging caused by environmental factors. The turning-point occurs in the menopause
(andropause). The estrogen receptor has been detected
on the cells of the skin. Accordingly, dermal cellular metabolism is influenced by the hypoestrogenoemic state of
menopause, leading to changes in the collagen content
and alterations in the concentration of glycoaminoglycans
(GAG). A reduction in hydrophilic glycosaminglycans
leads to a direct reduction in water content which influences the skin turgor. Decorin, the main proteoglycan in
skin, has a small size with a core protein of approximate-
ly 40kDa and one chondroitin sulfate / dermatan sulfate
glycosaminoglycan chain. The main function of decorin
is to regulate the collagen matrix assembly. Reducing the
length of the decorin, the GAG chain reduces the distance
between collagen fibrils. Collagen becomes sparser and
less soluble in intrinsically aged skin, but is thickened and
more soluble in extrinsically aged areas. Changes in skin
collagen lead to diminished skin strength.
Elastin, an important extracellular skin component,
degrades slowly and accumulates damage with intrinsic
aging. Increased synthesis of abnormally structured elastin occurs predominantly in photoexposed areas. This
leads to an age-related accumulation of aberrant elastoic
material clumped in the papillary dermis. Generally, age
leads to an increased folding and decreased interaction
of proteins with water. Despite increased GAGs in aged
skin, these are abnormally deposited on the elastoic material and cannot interact properly with water. Hence, in
aged skin, water is found in the tetrahedron form, bounded with similar rather than other molecules. Changes
in the macromolecular metabolism of the dermis are a
major factor leading to skin aging [1]. Specifically, the
accumulation of elastosis material is accompanied by
the degradation of matrix proteins, which is mediated by
matrix metalloproteinase (MMPs) in skin aging. Molecular alterations in the dermis include decreased collagen
synthesis, MMP induction, and abnormal accumulation
of elastic fibers and proteoglycans [2–4].
The accumulation of abnormal elastic material,
termed solar elastosis, is the prominent histopathologic
alteration in photoaged skin [5, 6].
Figure. Human skin biopsies: from young patient (panel A) and aged patient with atrophic epidermis and dermal papillae, and scarce blood vessels (panel B).
Stained with H & E, original magnification × 100. Ep – epidermis; De – dermis; arrows indicate some blood vessels
Skin aging
Lipid content appears to decrease with age, although
the proportion of different lipid classes remains fairly
constant [7]. A reduction of the microvasculature has
been observed in the skin of all elderly individuals
(Figure). Capillary blood flow velocity decreases significantly in postmenopausal women. Postmenopausal
flushing is due to profound vasodilatation in the dermal
papillae.
Hair growth is also influenced by the hormonal milieu, and consequently hair loss has been associated
with the beginning of menopause [8]. The increased
prevalence in the elderly of chronic wound-healing conditions, such as venous and diabetic ulceration, is firmly
established.
The ageing process, both intrinsic and extrinsic, is
also believed to be influenced by the formation of free
radicals, also known as reactive oxygen species.
Wrinkling and pigmentary changes are directly associated with photo-ageing and are considered its most
salient cutaneous manifestations. Skin aging and good
looking depend on a variety of factors: lifestyle, diet, heredity and personal habits. While no one can stop or even
slow down the intrinsic aging processes, everybody can
prevent and hide the external signs of premature aging
by protecting the skin from the sun, quitting smoking,
eliminating bad facial exercises, etc.
Tobacco smoking and skin aging
Epidemiological studies demonstrated that tobacco
smoking is one of the numerous factors contributing to
premature skin aging. Other factors include age, sex,
pigmentation, sun exposure history, and alcohol consumption [9–12]. Tobacco smoking exerts its deleterious effects on skin directly through its irritant components on the epidermis and indirectly on the dermis via
blood circulation [10, 13]. The decreased moisture in
the stratum corneum of the face contributes to facial
wrinkling due to direct toxicity of the smoke. Pursing
the lips during smoking with contraction of the facial
muscles and squinting due to eye irritation from the
smoke might cause the formation of wrinkles around
the mouth and eyes [14]. Boyd et al. have reported that
tobacco smoking enhances the effect of solar elastosis
in subjects averaging 42 pack-years of tobacco smoking [15]. In vitro studies using cultured skin fibroblasts
demonstrated that tobacco smoke extracts induce an
increase in tropoelastin. This too might be a cause of
premature skin aging.
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Hot climate and skin aging
The skin is a highly exposed organ during vacation
times, especially during travel to countries with subtropical and tropical climates. Prolonged stay in these countries significantly increases the risk of contacting rarely
seen dermatoses such as leishmaniasis, larva migrans and
myiasis. The bites of various flies may provoke itching
and excoriations that may be infected with Staphylococcus aureus and / or hemolytic streptococci, resulting
in impetigo, furunculosis or erysipelas. Elderly persons
spending weeks in the tropical sun may develop druginduced phototoxic or photoallergic rash due to concomitant medication for cardiovascular or rheumatic diseases.
Acute sunburn is considered a short-lasting problem, but
it increases the risk of malignant melanoma later. Mucocutaneous manifestations arising weeks and months after
returning from vacation should raise suspicions of sexually transmitted syphilis and HIV.
Disease-caused acceleration of skin aging
There is a broad and diverse spectrum of vasculitic
syndromes. These syndromes affect the skin with varying levels of associated systemic manifestations, running the gamut from a self-limited, localized, cutaneous
phenomenon to a rapidly progressive, multiorgan disease. The majority of cases of cutaneous vasculitis show
a neutrophilic small vessel vasculitis that can be either
a primary (idiopathic) disorder (e. g., cutaneous leukocytoclastic angiitis) or a secondary disorder associated
with drugs, infection (e. g., streptococcal infection, viral
hepatitis) or underlying disease (e. g., connective tissue
disease, malignancy) [16].
Sjögren’s syndrome (SS) is an autoimmune disease
characterized by exocrine gland involvement. The skin is
affected in nearly half of SS patients. Cutaneous manifestations consist of xerosis, angular cheilitis, eyelid dermatitis, pruritus, cutaneous vasculitis (frequently manifesting as palpable purpura), and erythema annulare. Most
of them are nonspecific and less severe than the oral,
ocular, or musculoskeletal symptoms [17]. Skin manifestations can be observed in autoimmune diseases such
as rheumatoid arthritis (RA), dermatomyositis (DM) and
Behçet syndrome (BS). In RA, the most widely recognized skin lesion is the rheumatoid nodule. Other cutaneous manifestations can be observed either as non-specific
or related to the disease itself and / or to the commonly
used drugs. In DM, skin manifestations are frequent and
include a heliotrope rash (blue-purple discoloration) on
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the upper eyelids with edema, a flat red rash on the face
and upper trunk, and erythema of the knuckles with a
raised violaceous scaly eruption (Gottron rash). The most
typical skin manifestations are nodular lesions which are
commonly seen in BS and may be due to panniculitis
(erythema nodosum (EN)-like lesions) or superficial
thrombophlebitis [18].
Skin aging in progeria
Progeria, also known as the Hutchinson–Gilford syndrome, is an extremely rare inborn condition, initially
reported by Johnathan Hutchinson in 1886 and further
described by Hastings Gilford in 1904. Transmission is
most likely from a sporadic autosomal dominant mutation. The patients usually appear normal at birth. Clinical
manifestations are evident by the first or second year of
life and include the physical characteristics usually associated with the elderly. Histopathologic changes occur
primarily in the skin, bone, and cardiovascular tissues,
while other organs appear to be unaffected. Current research suggests a genetically based underlying defect of
hyaluronic acid that may possibly account for the entire
process. Werner’s syndrome (adult onset progeria) is also
a rare form of autosomal recessive genodermatosis associated in almost 80% of cases with mutation of the WRN
gene. Rapid aging syndrome is characterized by a short
stature with skin and hair anomalies (early graying of
the hair, alopecia, depilation, sclerosed skin), orthopedic
complications (flat foot, hallux valgus and other joint deformations) as well as systemic signs (early cataract, premature and diffuse atherosclerosis, endocrinopathies [19,
20] and a high risk of certain types of cancer (sarcomas,
myeloid blood dyscrasias).
Principles of the aged skin care
The dramatic increase in the aging population and the
psychosocial impact of skin aging has created a demand
for effective interventions. Intrinsic and extrinsic aging
of the skin follow different pathways, but the end result
is similar. Treatment options include cosmeceuticals,
laser rejuvenation, chemical peels, and microdermabrasion. The advances that have been made in the past 25
years in the understanding of the clinical, biochemical,
and molecular changes associated with aging have led to
the development of many different approaches to reduce,
postpone, and in some cases repair the untoward effects
of intrinsic programmed aging and extrinsic environmental injury [21]. The architectural frameworks of the skin
microcirculation are rather complex and change continuously with aging. In females, this decline in the effectiveness of skin repair mechanisms follows the menopause,
and a series of clinical studies have identified estrogens as
endogenous enhancers of healing processes. The administration of 17 beta-estradiol, either systemically or topically, has been shown to reverse the fundamental repair
defects observed in postmenopausal women. By contrast,
androgenic species retarded repair and interfered with
the accumulation of the structural proteins that reconstitute the damaged dermis. Since estrogen-based hormone
replacement therapy produces wide-ranging effects, not
all of which are considered to be desirable, more recent
studies have sought to identify downstream mediators of
estrogenic effects in order to formulate better targeted
strategies for improving skin repair in the elderly [22].
Preventing the effects of extrinsic aging involves using
sunscreen – the right product used in the right amount,
at the right time, in the right places [23]. Different cosmeceuticals include antioxidants, growth factors, peptides, anti-inflammatories / botanicals, polysaccharides,
and pigment-lightening agents.
The correct use of moisturizers and cleansers is an
integral component of the skin care regimen for any
patient with skin problems. When used appropriately,
these products not only improve skin hydration by reducing transepidermal water loss, but also help to restore
the skin barrier and improve the aesthetic appearance of
the skin. Proper moisturizing and cleansing are essential
components of an overall skin treatment plan to ensure a
satisfactory outcome in patients [24].
Growth factors, in addition to their crucial role in cutaneous wound healing, are also beneficial for skin rejuvenation. The antiaging effects of some skin creams
is based on a mixture of human growth factors and cytokines, which was obtained through a biotechnology
processes using cultured human fetal fibroblasts. Topical application of growth factors and cytokines is beneficial in reducing external signs of skin aging [25]. The
response to cosmetic treatment modalities differs in patients of a darker skin pigmentation, and this needs to be
recognized by the cosmetic and laser surgeon.
Antioxidants protect the cells from the damaging effects of oxygen-free radicals. Antioxidants include vitamins A, C, E and betacarotene, and are available in ointment, cream, lotion, and oral supplement forms. Some
people use a vitamin-A based cream, or creams containing alpha-hydroxy acids, to diminish the appearance of
Skin aging
age spots and wrinkles. Laser treatments and bleaching
are other options for removing age spots. Frequent moisturizing with an over-the-counter cream or lotion can
relieve dry, itchy skin. Some conditions of aging skin,
such as seborrheic keratoses, broken blood vessels, and
purpura require no treatment. However, they can be removed or their appearance diminished if they become
irritated or are unsightly. Actinic keratoses are removed
from the skin.
Dermabrasion, laser resurfacing, chemical peeling,
and some topical treatments can influence skin, giving it
a smoother and refreshed appearance. Treatments administered for menopause, in particular hormone replacement therapy, alter its effects on the basic components
of the skin. In conclusion, specific care and treatment do
not stop natural aging processes in the skin, nevertheless, they can dramatically change the external sings of
aging.
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ODOS SENĖJIMAS
atsiranda smulkių raukšlių, oda plonėja, tampa permatoma,
pigmentuota, sukritusi, sausa, išvagota.
Neįmanoma sustabdyti odos senėjimo, sąlygoto vidinių
procesų, tačiau jį galima sulėtinti, apsisaugant nuo saulės, nerūkant, vengiant žalingos mimikos, gydant odą veikiančias ligas.
Z. Mackiewicz, A. Rimkevičius
Santrauka
Negrįžtami odos pakitimai atsiranda gyvenimo trečiajame dešimtmetyje, tačiau jie dar ilgai lieka nepastebimi. Odos
senėjimas – tai sudėtingas biologinis procesas, veikiamas genetinės organizmo programos bei išorinių veiksnių: veido mimikos, netinkamos padėties miegant, rūkymo ir kitų. Senstant
Received 14 November, 2007
Accepted 27 March, 2008
Raktažodžiai:
oda, senėjimas